This thesis discusses the balance between accepting or rejecting proposals of interactions between microbes and plants. Plants cannot move, so once a seed germinates plants are destined to stay where they are. Plants thus experience heavy selection pressure in their environments, and many traits have evolved to permit plants to succeed across the globe. This selective pressure can be divided into abiotic and biotic stresses. Abiotic stresses such as temperature, sunlight, drought and salinity will not be discussed here. Biotic stresses occur when other organisms cause damage to the plants. These can be virus-, bacteria- or fungal attacks or grazing by insects or higher animals. In this thesis, two cases of plant-bacterial interactions will be discussed, as well as a special case concerning plant metabolism related to their responses to biotic stresses.
The first case focused on the biochemical pathway by which pathogenic bacterial interactions leads to plant resistance and to host cell death. In this case I sought to uncover the mystery of plant-programmed cell death in the Hypersensitive Response (HR) following the recognition of the Gram-negative bacteria Pseudomonas syringae by the plant Arabidopsis thaliana. The HR ultimately leads to host cell death, a defense mechanism whereby the plant sacrifices the attacked cells, thus preventing the bacteria from spreading into other parts of the plant. This event has been discussed since the turn of the millennium, when the fully sequenced genome of A. thaliana was released. Interestingly, when the genome was searched for homologs of metazoan apoptotic genes, none were identified. It was surprising that apoptosis apparently does not take place in plants since, as we all know, deciduous trees shed their leaves, hence the Greek word ”apoptosis”, meaning ‘leaf shedding’. My colleagues and I pursued reverse genetic approaches to uncover an alternative pathway leading to programmed cell death in infected plant cells.
The second case discussed is also related to plant stress, and continues work from our group on the A. thaliana ACCELLERATED CELL DEATH (ACD) 11 null mutant first described by Brodersen et al., 2002. The acd11 null mutant does not survive into adulthood and undergoes systemic, programmed cell death PCD before it flowers to produce seed for the next generation. This PCD is dependent on signalling hormones related to plant defense, and can be suppressed by secondary, non-allelic mutations. Therefore, approaches to understand the function(s) of ACD11 include the identification of suppressors and analyses of the ACD11 protein interaction network. I exploited this latter approach and describe here ACD11 protein interactions and the subcellular localization of these interactors.
The third case presented here relates to the initial phase of plant-microbe interaction in which plants recognize specific soil bacteria. My aim was to better understand receptor–ligand interactions between the Gram-negative bacteria Mesorhizobium loti and the legume Lotus japonicus. This event leads to a symbiosis between the two organisms that have a dramatic effect on the plant’s ability to acquire inorganic nitrogen. Furthermore, I was interested in what happened inside the plant once the receptor was triggered, more specifically what proteins were activated in the signalling cascade following receptor triggering.